Turning cancer cell dependencies into targeted therapies

Beyond Biotech - the podcast from Labiotech
Welcome to the official Labiotech.eu podcast - Beyond Biotech! Each week, we talk about what's happening in the world of biotech, with news and interviews with experts from companies around the world. Join us as we cover the latest news, breakthroughs and innovations shaping the life sciences industry.A new podcast episode is available every Friday. The host is Dylan Kissane.
Beyond Biotech - the podcast from Labiotech
Turning cancer cell dependencies into targeted therapies
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Today I’m delighted to welcome Andy Parker, CEO of Step Pharma.
With over 25 years of experience across AstraZeneca, Shire, Zealand Pharma, and
venture capital, Andy has led Step Pharma since 2019. The company is pioneering
a targeted approach to cancer and blood disorders by inhibiting the enzyme
CTPS1. Their lead candidate, dencatistat, blocks this pathway that certain
cancer cells and activated immune cells rely on, while sparing healthy cells
that use the related CTPS2 enzyme.
In this episode, we’ll dive into the science behind this mechanism, explore Step
Pharma’s expanding pipeline from lymphomas and solid tumours to essential
thrombocythaemia, and discuss their recent €38 million Series C financing.
We’ll also look ahead to the future of precision oncology.
- 01:17 Meet Andy Parker
- 06:12 The biotech ecosystem around Geneva
- 07:51 The CTPS1 enzyme and why cancer cells depend on it
- 14:08 Pipeline-in-a-product strategy across three indications
- 20:14 The series C: €38 million raise
- 25:41 Partnering with big pharma: possibilities and limits
- 28:11 The future of precision oncology and metabolic targeting
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To dive deeper into the topic:

Facts Only

Andy Parker is the CEO of Step Pharma.
Step Pharma pioneered a targeted approach to cancer and blood disorders by inhibiting the enzyme CTPS1.
The lead candidate, dencatistat, blocks the pathway relied upon by certain cancer cells and activated immune cells.
dencatistat spares healthy cells that use the related CTPS2 enzyme.
Step Pharma's pipeline covers lymphomas, solid tumors, and essential thrombocythaemia.
The company raised €38 million in Series C financing.
The podcast will cover the mechanism of CTPS1 dependency, the pipeline strategy across three indications, and precision oncology.

Executive Summary

Andy Parker, CEO of Step Pharma, has been involved in the development of a targeted approach to cancer and blood disorders by inhibiting the enzyme CTPS1. The company's lead candidate, dencatistat, functions by blocking the pathway that specific cancer cells and activated immune cells depend on, while sparing healthy cells that utilize the related CTPS2 enzyme. Step Pharma possesses an expanding pipeline targeting lymphomas, solid tumors, and essential thrombocythaemia. The company recently secured €38 million in Series C financing. The discussion will explore the underlying science of the mechanism, the scope of the pipeline across various indications, and the implications for precision oncology.

Full Take

The narrative centers on the concept of metabolic targeting within oncology, specifically leveraging differential enzyme dependency (CTPS1 vs. CTPS2) to achieve therapeutic selectivity. The focus shifts from broad cytotoxic treatments to disrupting essential dependencies unique to pathological cells. This structure suggests a powerful pattern aimed at re-framing disease as an exploitable biochemical imbalance rather than simply a mass of abnormal cells. The progression from understanding the mechanism (CTPS1 dependency) to applying it across a pipeline (three indications) and securing significant capital highlights a common trajectory in modern biotech: identifying a unique biological vulnerability, developing a highly specific modulator, and scaling that modulation across multiple disease states. The discussion around partnering with large pharmaceutical companies introduces the friction between targeted science and commercial reality—the limits of specificity versus market viability. A key tension emerges regarding how much precision oncology can truly capture the complexity of systemic diseases like blood disorders alongside solid tumors, prompting an underlying question about whether targeting a single enzyme pathway offers true systemic control or merely incremental advantage.

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